Secondary Osteonecrosis of the Knee

Etiology

SON is caused by an interruption of the blood supply to the subchondral bone due to various predisposing factors or conditions.[4][5] Unlike SONK, which has no clear risk factors, SON is strongly associated with many direct and indirect causes that lead to bone ischemia. Major risk factors include:

• Glucocorticoid (corticosteroid) use: Chronic or high-dose steroid therapy is 1 of the most common causes of SON. Corticosteroids are implicated in over 90% of SON cases. They are thought to cause enlargement of bone marrow fat cells, increase intraosseous pressure, and induce lipid metabolism disturbances, ultimately compromising blood flow to bone. Steroid-induced hyperlipidemia and thrombosis may further contribute to avascular necrosis.[6]
• Alcohol abuse: Excessive alcohol intake, similar to steroids, is present in most cases. Alcohol can increase fatty deposition in the marrow and coagulation abnormalities, leading to vessel occlusion.
• Obesity and metabolic factors: Obesity is an indirect risk factor that may worsen intraosseous hypertension and contribute to vascular insufficiency. Additionally, conditions like hyperlipidemia or Cushingoid features from steroid use can compound risk.
• Hemoglobinopathies and coagulopathies: Sickle cell disease is a well-documented direct cause of osteonecrosis due to the sickling of red blood cells, which leads to vaso-occlusion in the bone’s microcirculation. Other hemoglobinopathies or coagulation disorders can have similar effects.[7]
• Myeloproliferative disorders: Conditions such as leukemia or myeloproliferative neoplasms can contribute to SON, possibly by increasing marrow cell turnover and local pressure, or by direct leukemic infiltration, which disrupts blood flow.
• Gaucher disease: This lysosomal storage disorder causes the accumulation of glucocerebrosides in bone marrow macrophages, leading to marrow expansion and interference with blood supply, which predisposes bone to avascular necrosis.
• Systemic lupus erythematosus and autoimmune disease: Osteonecrosis in patients with lupus is often attributed to chronic corticosteroid therapy; however, systemic lupus erythematosus and antiphospholipid antibodies may contribute to a hypercoagulable state. Young patients with lupus on steroids are at particularly high risk of multifocal osteonecrosis.
• Organ transplantation and chronic renal failure: Transplant recipients often require prolonged corticosteroid and immunosuppressive therapy, increasing the risk of osteonecrosis. Chronic dialysis has also been associated with osteonecrosis, possibly due to secondary hyperparathyroidism and metabolic factors.
• Chemotherapy and radiation: Certain chemotherapeutic agents can damage microvasculature or bone cells. Radiation therapy can cause avascular necrosis in the treatment field, though it usually affects bone directly irradiated rather than a typical SON distribution.
• Dysbaric conditions: Decompression sickness in divers (dysbaric osteonecrosis) can cause nitrogen emboli in subchondral vessels, typically affecting the femur and humerus.
• Smoking: Tobacco use has vasoocclusive and prothrombotic effects that may contribute to SON, though it is often a co-factor with other risks rather than a primary cause of osteonecrosis.

The unifying mechanism in these diverse conditions is the impairment of bone blood flow, resulting in the cellular death of bone marrow and osteocytes. The loss of viable bone triggers reparative processes that cannot keep pace with bone resorption, ultimately leading to structural weakness and collapse of the subchondral bone. No inherited genetic predisposition to SON has been identified; rather, 1 or more acquired risk factors underlie most cases. In many patients, multiple risk factors (eg, a patient with lupus on steroids and immunosuppressants) act synergistically to precipitate osteonecrosis.[7][8]

Epidemiology

SON is often underdiagnosed, as it may remain asymptomatic until advanced stages. As a result, SON can be overlooked in patients with concurrent joint conditions, such as hip osteonecrosis, which may mask or divert attention from knee-related symptoms. Some patients may present later with end-stage knee osteoarthritis without a recognized earlier phase of osteonecrosis. Therefore, awareness of at-risk populations, such as young patients on chronic steroids, is crucial for early identification. The knee is the second most common joint affected by osteonecrosis after the hip.[9] Overall, osteonecrosis of the knee (all types) is less frequent than osteonecrosis of the femoral head; knee involvement is about 10% of all osteonecrosis cases and roughly 90% lower than the incidence in hips. Among the types of knee osteonecrosis, SONK is the most common, whereas SON accounts for the second most common subtype.[10][11][12]

SONK typically presents in the 6th decade of life (50s to 60s) and is more common in women than men. This condition usually involves a single knee and most often a single lesion in the medial femoral condyle. Patients often report an acute or subacute onset of knee pain without trauma. SONK is not associated with risk factors like steroid use, and it generally does not occur in multiple joints. Small lesions in SONK can sometimes be self-limited or respond to conservative management, whereas larger lesions may progress to collapse.[13]

SON is rarer than SONK, and usually affects patients younger than 45. Unlike SONK, there is no strong sex predominance in all series; however, some literature suggests women may be slightly more affected than men, possibly due to underlying diseases like lupus.[14] The lateral femoral condyle is frequently involved in SON. Study results indicate the lateral condyle is affected alone or along with the medial condyle in up to 60% of cases, contrasting with SONK, which classically involves the medial condyle. Moreover, SON often involves both femoral condyles and can extend beyond the epiphysis into the metaphysis or diaphysis of the distal femur and the tibial plateau. Bilateral knee involvement is frequently seen in SON, affecting approximately 30% to 80% of cases. Other joints—particularly the hips—are commonly affected in many patients. The femoral head is reportedly involved in over 90% of cases of SON of the knee, reflecting the multifocal nature of secondary osteonecrosis.[15][16]

History and Physical

Patients with SON typically present with knee pain of insidious onset, as opposed to the sudden, sharp pain often described in SONK. The pain is usually localized to the affected condyle and tends to be dull, aching, and progressive.[15][17] A high index of suspicion in patients with known risk factors who present with knee pain is critical. Because SON often affects multiple joints, examination of the hips and other painful joints should also be performed. Key features of SON include:

• Demographics and risk factor history: Patients are often younger than 45 and have a history of risk factors such as corticosteroid use, alcohol abuse, or clotting disorders. Many have bilateral symptoms or concurrent hip or groin pain, which may suggest hip osteonecrosis.
• Pain characteristics: Knee pain typically develops gradually and worsens over weeks to months. Early on, pain may be mild and only with activity, but can progress to occur at rest and night.
• Laterality: SON frequently involves both knees. If only 1 knee is symptomatic, evaluation of the other knee is still warranted.
• Associated symptoms: Patients might also mention hip or shoulder pain, reflecting possible osteonecrosis in other joints.

On physical exam, early-stage SON can be subtle. Common findings include:

• Tenderness: Localized tenderness upon palpation over the affected femoral condyle is the most consistent finding.
• Joint effusion: A small to moderate effusion may occur, especially if subchondral collapse has started.
• Range of motion: Usually well-preserved early on. Pain at extremes of flexion or deep knee bending may be observed.
• Crepitus/mechanical signs: Generally absent in early SON unless there is collapse causing irregularity in the joint surface.
• Gait: Patients may exhibit an antalgic gait by limiting weight-bearing on the affected side. In bilateral cases, a slow, cautious gait is common.

Evaluation

The diagnosis of SON is confirmed through imaging, with magnetic resonance imaging (MRI) being the gold standard for early detection.[2]

Imaging Studies

• Plain radiograph (x-ray)
  • Initial evaluation of chronic knee pain typically includes weight-bearing anteroposterior and lateral knee radiographs. In early-stage SON (Ficat stage I), x-rays may appear normal. As the disease progresses to stage II, subtle changes, such as sclerosis or cystic lesions in the subchondral bone, may become visible.
  • In more advanced stages, one may observe the crescent sign (a subchondral radiolucent line indicating impending collapse) or frank flattening and collapse of the femoral condyle (stage III), and eventually, joint space narrowing with secondary osteoarthritic changes (stage IV). Given SON's often multifocal and bilateral nature, radiographs of the contralateral knee and possibly hips should be considered if symptoms or risk factors are present.
• MRI
  • The diagnostic modality of choice for knee osteonecrosis is MRI, which can detect bone marrow edema and subchondral lesions before x-ray changes are appreciable. In a study by Mont et al, MRI identified 100% of knee osteonecrosis lesions in symptomatic individuals, whereas bone scans detected only 64%, and plain radiographs detected even fewer lesions. MRI findings in SON typically include a geographic area of subchondral T1 hypointensity and T2 heterogeneity, often with surrounding bone marrow edema.
  • A characteristic finding for osteonecrosis is the “double line sign” on T2-weighted images. The double line sign is created by an inner bright line of granulation tissue and an outer dark line of sclerotic bone, though this is more often described in femoral head avascular necrosis. In SON, a demarcation rim or double-halo sign was noted on the MRI. Narváez et al reported that the rim sign, adjacent to the necrotic area, was present in 70% of SON cases and 0% of spontaneous cases, potentially helping to distinguish SON from SONK on imaging.
  • Additionally, the distribution of edema in SON on MRI can span the epiphysis, metaphysis, and diaphysis of the bone. In contrast, the edema is typically confined to the subchondral region of 1 condyle in SONK. Thus, MRI not only confirms the diagnosis and extent of lesions but may also suggest a secondary versus primary etiology based on the pattern of involvement.[18] 
• Bone scan (nuclear medicine)
  • Technetium-99m bone scintigraphy was previously used to identify osteonecrosis lesions and multifocal disease; however, it has largely been supplanted by MRI due to its superior sensitivity and specificity. Bone scans are sensitive in later stages of osteonecrosis, but lack specificity and may not identify early lesions. Given MRI’s superiority, bone scans are generally not indicated for routine diagnosis of SON. Bone scans may be useful when MRI is contraindicated or unavailable, and can also aid in whole-body evaluation for multifocal disease when necessary.[18] 
• Computed tomography scan
  • Although not routinely required for diagnosing SON, computed tomography (CT) can provide detailed visualization of subchondral fractures or bone collapse. CT scans can be helpful in presurgical planning, particularly when subchondral collapse is suspected or to assist in decisions about bone grafting.[19]

Laboratory Studies

Although no specific laboratory tests exist for diagnosing osteonecrosis, laboratory work is valuable for identifying potential underlying causes. Patients without a known diagnosis should be evaluated for conditions such as coagulopathies (eg, antiphospholipid antibodies, protein C/S deficiency), inflammatory diseases (eg, antinuclear antibody for lupus), or metabolic issues if clinical suspicion arises. In known cases (eg, lupus on steroids), labs directly guide the management of the underlying disease, but not the osteonecrosis itself. Joint infection or inflammatory arthritis should be ruled out if signs like significant warmth, redness, or very high inflammatory markers are present. SON typically exhibits only mild elevation of inflammatory markers, if any.[19]

Treatment / Management

The primary goal in managing SON is to slow or halt disease progression while preserving the native joint for as long as possible.[20] Management is based on the disease stage and the patient's clinical condition. The current standard of care for the treatment of SON emphasizes early joint-preserving interventions, because SON typically affects younger patients and can lead to devastating arthritis.[21] 

Unfortunately, no "gold standard" treatment for SON exists; management requires a tailored approach.[22] Conservative treatments alone fail to prevent progression in most cases. While conservative therapy is useful for the treatment of early disease, it often only delays the need for joint replacement in cases of aggressive secondary osteonecrosis. One series reported that about 80% of patients initially treated nonoperatively with protected weight-bearing and medications progressed to require total knee arthroplasty (TKA) within 6 years.

Standard Stage-Based Algorithm Approach

• Stage I and II (pre-collapse): First-line treatment is usually nonoperative in asymptomatic or minimally symptomatic cases. Treatment includes protected weight-bearing and medical therapy, as discussed in the next section. However, given that many patients have progressively worsening pain or risk factors for progression of osteonecrosis, early surgical intervention may be considered as soon as stage II if the lesion is large or symptoms are severe. In patients with pre-collapse lesions who fail conservative measures or have high-risk lesions, joint-preserving surgical options such as core decompression, drilling, or bone grafting are indicated to try to prevent collapse.
• Stage III (early collapse, small area): If subchondral collapse is minimal—particularly with small lesions and minor joint surface depression—joint-preserving procedures, such as osteochondral grafting or focal osteotomy, may still be viable options. However, arthroplasty is recommended for extensive collapse or a large lesion. Importantly, in secondary osteonecrosis, collapse often involves both condyles or a large portion of the joint, making partial replacement a less suitable option.
• Stage IV (advanced collapse/arthritis): The standard of care is surgical joint replacement; arthroplasty reliably alleviates pain and restores function in cases of stage IV disease. In younger patients, every effort is made to delay TKA until necessary, due to the finite lifespan of prosthetic implants and the potential need for future revision surgeries. When TKA is performed for SON, advanced techniques like cemented components, stem extensions, or augments have demonstrated excellent results, comparable to those achieved in TKA for primary osteoarthritis.

Nonoperative Management

Conservative management is mainly indicated in stage I or II osteonecrosis and for patients with small lesions or those who are poor surgical candidates. The goals of conservative treatment are to relieve pain, reduce load on the affected bone, promote any possible healing, and prevent or delay collapse. Key components of nonoperative management include:

• Protected weight-bearing: Offloading the affected knee reduces mechanical stress on the necrotic area. This often involves using crutches, a walker, or a cane and limiting weight-bearing on the affected leg (toe-touch or partial weight-bearing) for several weeks or months. A period of protected weight-bearing (eg, 6 to 12 weeks) is advised in early SON to assess whether symptoms improve and to allow the lesion to stabilize. Strict rest may help small lesions heal or prevent propagation of a subchondral fracture. Modifying activities by avoiding high-impact movements, prolonged standing, and stair climbing is recommended. Quadriceps strengthening and range-of-motion exercises, as tolerated, are encouraged to maintain muscle support and joint function without impact loading.
• Analgesic and anti-inflammatory medications: Nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen are commonly used to manage pain and inflammation. NSAIDs can help relieve pain and reduce inflammation in the bone and surrounding tissues, potentially alleviating bone marrow edema. While NSAIDs do not modify the disease course, they improve comfort and function during the observation period.
• Bisphosphonates: Bisphosphonate medications, such as alendronate, have been explored for treating osteonecrosis due to their ability to inhibit osteoclast-mediated bone resorption. Bisphosphonates may slow the collapse of necrotic bone, allowing more time for repair. The results of some studies, mostly on femoral head avascular necrosis, suggest that bisphosphonates can reduce the rate of collapse and improve symptoms. In SON of the knee, bisphosphonates have shown promise in promoting healing of subchondral fractures and improving radiographic appearance in early stages; however, data are limited, and their use is off-label. Bisphosphonates may be considered, especially if osteopenia or osteoporosis coexist.
• Prostaglandin analogues (Iloprost): Iloprost is a prostacyclin (PGI2) analog with vasodilatory and antiplatelet effects. Intravenous iloprost has been used to treat bone marrow edema syndromes and early osteonecrosis to improve microcirculation. Study results have reported that iloprost can lead to symptom improvement in most patients with early osteonecrosis. In a series of 108 patients (136 joints) with avascular osteonecrosis of various joints treated with iloprost, 74.8% of patients reported significant improvement in pain. However, many advanced cases still proceeded to arthroplasty, as 71% of stage III and 100% of stage IV lesions required joint replacement despite iloprost treatment. Iloprost is typically given as a series of daily infusions over 5 to 7 days and may be considered in early SON (stage I or II), particularly if there is substantial bone marrow edema on MRI.
• Physical therapy and biophysical modalities: Physical therapy focuses on maintaining joint range of motion, muscle strength (especially the quadriceps and hip abductors for knee support), and using gait aids properly. In addition, the following biophysical stimulation techniques have been studied:
  • Pulsed electromagnetic field therapy: This therapy involves applying electromagnetic fields to the affected area; some study results have shown that stimulating osteogenesis from this type of therapy potentially reduces inflammation. Research on hip osteonecrosis suggests that pulsed electromagnetic field therapy, when combined with core decompression, improves outcomes compared to core decompression alone. In cases of SON of the knee, results from a study found that pulsed electromagnetic field therapy significantly reduced knee pain and the size of the necrotic lesion at 6 months, and helped avoid surgery in 86% of treated knees at 24 months.
  • Extracorporeal shock wave therapy: The application of low-energy shock waves to bone has been proposed to promote revascularization. In cases of femoral head osteonecrosis, extracorporeal shock wave therapy has shown potential in improving symptoms and delaying collapse. The role of extracorporeal shock wave therapy in SON of the knee is not well-established, but it is a noninvasive treatment option that can be used in the early stages of the disease.
  • Hyperbaric oxygen (HBO) therapy: HBO involves breathing 100% oxygen in a high-pressure chamber, which increases oxygen delivery to tissues; this therapy is thought to enhance oxygenation of ischemic bone and support healing. HBO is an approved adjunct treatment for certain ischemic bone conditions, and some studies' results have reported improved outcomes in early-stage femoral head osteonecrosis with its use. For knee lesions, case reports (eg, by Bosco) have shown symptom relief after HBO therapy. However, HBO therapy is logistically challenging and expensive, and no randomized trials have confirmed its effectiveness in treating SONK or SON.
• Lifestyle modifications: Addressing risk factors contributing to osteonecrosis development is crucial. Patients are advised to stop smoking, avoid alcohol, maintain a healthy weight to reduce knee load, and control lipid levels if elevated. If SON is steroid-induced and the clinical situation allows, reducing the dose or using alternate therapies, with the prescribing clinician's guidance, can potentially slow further osteonecrosis. Optimizing control of underlying diseases, such as lupus activity, is also crucial in minimizing the need for high-risk medications.

The current standard of care for SON follows a stage-appropriate management strategy, which includes conservative treatment for early-stage disease, early surgical intervention for progressive or larger lesions to preserve the joint, and arthroplasty for late-stage disease. This approach aims to maximize knee function and longevity, delaying joint replacement until necessary while ensuring optimal outcomes when performed. Conservative management, which includes joint offloading, pain control, pharmacological agents such as bisphosphonates or iloprost, and adjunctive biophysical therapies, can provide symptomatic relief and potentially slow the progression of the disease. However, the success of conservative management is limited, as no large randomized trials support its efficacy.

Much of the available evidence is derived from smaller studies or extrapolated from data on hip osteonecrosis. A review by Boontanapibul et al reported that around 80% of patients with osteonecrosis who received nonoperative treatment eventually progressed to advanced stages that required surgical intervention. As a result, conservative treatment is primarily a temporizing measure for early-stage disease. Patients on nonoperative therapy require close monitoring with periodic clinical exams and imaging to detect lesion enlargement or impending collapse. If the disease progresses, timely surgical intervention is necessary to optimize joint preservation and long-term outcomes.

Surgical Treatment and Outcomes

Surgical management is the cornerstone of treatment for SON, especially given the high failure rate of purely conservative measures in this condition. The choice of procedure depends on the stage of disease, size and location of the lesion, and patient factors (such as age and activity level). Broadly, surgical options are divided into joint-preserving surgeries aimed at preventing collapse and "buying time" before arthroplasty and partial or total joint replacement for advanced disease.

Joint-Preserving Surgical Options

Joint-preserving procedures are typically indicated in pre-collapse stages (I and II) or sometimes in early stage III if the collapse is minimal and the patient is young.[23] The goal is to relieve intraosseous pressure, promote revascularization and healing of the necrotic bone, and maintain the native joint as long as possible. Key procedures include:

• Core decompression and drilling: Core decompression involves drilling 1 or more channels into the necrotic area of bone to reduce intraosseous pressure and create channels for new blood vessels. This procedure can be performed percutaneously under fluoroscopic or computed tomography guidance, typically by drilling from the anterolateral distal femur into the affected condyle, maintaining an extra-articular approach. Mont and colleagues reported excellent outcomes with a percutaneous multiple small drill-hole technique in SON, achieving clinical improvement in 92% of cases at 3-year follow-up.[24][25] This minimally invasive approach demonstrated low morbidity and effectively delayed the need for TKA in many patients.
• Marrow-stimulation techniques (microfracture/drilling): Similar to techniques used for focal cartilage defects. Arthroscopic drilling or microfracture of the lesion stimulates a healing response from marrow elements. Studies suggest better outcomes are achieved when scaffold augmentation is used in conjunction with microfracture rather than alone.[26]
• Osteochondral autograft or allograft transplantation: This approach addresses both bone loss and cartilage surface defects. The osteochondral autograft transfer system uses the patient’s cartilage and bone, whereas allografts use cartilage and bone from cadaveric donors. The osteochondral autograft transfer system is typically used for small to medium-sized lesions (less than 3-4 cm²).
• Autologous chondrocyte implantation with bone grafting (sandwich technique): A 2-stage procedure that involves harvesting cartilage cells and possibly bone grafting the defect, followed by the implantation of cultured chondrocytes.
• Debridement and bone marrow concentrate injection/grafting: Necrotic bone is debrided, and the defect is filled with concentrated bone marrow aspirate rich in mesenchymal stem cells. Several studies have reported significant symptom relief and delayed disease progression using bone marrow concentrate injections.
(A1)

Joint Replacement Surgery

For advanced secondary osteonecrosis (stage III with significant collapse, or stage IV), or for cases that fail joint-preserving treatments, arthroplasty is recommended. Despite challenges, complication rates of TKA in SON are low, and outcomes approach those seen in primary osteoarthritis.[27][28]

• Unicompartmental knee arthroplasty: This procedure resurfaces only the affected compartment (medial or lateral); therefore, unicompartmental knee arthroplasty is better suited for SONK with isolated medial or lateral disease. SON often involves multiple compartments, limiting the utility of unicompartmental knee arthroscopy.
• TKA: The treatment of choice for advanced secondary osteonecrosis involving multiple compartments or large lesions. Modern series have shown excellent outcomes, with implant survival rates around 92% at 6 to 10 years. Due to the typically young age of many individuals with SON, long-term monitoring is essential.

Emerging Treatments and Future Directions

Research continues into better joint-preserving therapies and earlier interventions, including:

• Cell-based therapies (stem cells): Mesenchymal stem cell (MSC) injections or bioengineered scaffolds seeded with MSCs are under investigation.[29][30]
• Tissue engineering and biomaterials: Advanced scaffolds and single-stage surgeries combining microfracture, MSC application, and scaffold use are being explored.
• Pharmacological agents: Investigations are underway into bisphosphonates, statins, and anticoagulants to prevent SON progression.
• Improved imaging and biomarkers: Advanced MRI techniques and serum markers may enable earlier diagnosis.
• Preventive strategies: Lower effective steroid doses, steroid-sparing immunosuppressants, and prophylactic measures in high-risk populations.
(B3)

Differential Diagnosis

The evaluation must consider other causes of knee pain and radiographic lesions.[2][4] Important differentials include:

• SONK: This condition is distinguished by older age, usually single-condyle involvement, no risk factors, and often acute onset.
• Osteochondritis dissecans: This condition typically occurs in teenagers and young adults and involves subchondral bone fragmentation, usually in the lateral aspect of the medial femoral condyle. Osteochondritis dissecans lesions are generally smaller and exhibit distinct MRI characteristics, often appearing as a fragment with potential instability.
• Insufficiency or stress fractures: Particularly in osteoporotic patients, subchondral insufficiency fractures can mimic SONK clinically and on MRI due to the presence of bone marrow edema. In secondary osteonecrosis, patients are typically younger and often present with identifiable risk factors. MRI often reveals a necrotic focus with a well-defined rim, which helps differentiate it from other conditions.
• Degenerative joint disease (osteoarthritis): Chronic knee osteoarthritis can lead to subchondral bone changes and cysts, whereas primary osteoarthritis is characterized by osteophytes and joint space narrowing as primary features. SON can secondarily cause osteoarthritis.
• Inflammatory arthritis: Conditions like rheumatoid arthritis can cause knee pain and bone erosions; however, they typically exhibit distinct clinical and imaging patterns, such as erosions in the juxtaarticular bone and synovitis on MRI.
• Bone tumors or tumor-like lesions: These are typically distinguished on MRI by their unique signal characteristics and the absence of the classic patterns seen in osteonecrosis.

Staging

Staging and Classification

Accurate staging of SON helps clinicians determine disease severity and guide management decisions.[20][31] Two main classification systems are used for osteonecrosis of the knee:

• Koshino classification: Developed in 1979 for SONK, this classification has 4 stages based on radiographic and clinical findings. Koshino staging is more historical for idiopathic SONK, and while it can describe SON, it doesn’t account well for multifocal lesions.
  • Stage I: Knee symptoms are present, but radiographs are normal (occult lesion). At this stage, an MRI or bone scan may detect the lesion.
  • Stage II: Radiographs show sclerosis or cystic lesions in the subchondral bone, often with flattening of the affected condyle and subchondral radiolucencies without collapse. Surrounding reactive osteosclerosis may be present.
  • Stage III: Progressive changes with extension of the radiolucent area and subchondral collapse. The classic crescent sign may be visible, indicating a loss of bone structural integrity.
  • Stage IV: End-stage disease characterized by degenerative changes, including joint space narrowing, secondary osteophyte formation, and subchondral sclerosis; essentially osteoarthritis secondary to the osteonecrosis.
• Modified Ficat and Arlet classification (for the knee): The Ficat and Arlet system was originally developed for osteonecrosis of the femoral head; however, a modified version has been adapted for use in the knee. The modified Ficat system is widely used in clinical practice for staging knee osteonecrosis. In practice, staging is determined by imaging (x-ray ± MRI findings) in conjunction with symptoms. The early stages (I and II) are characterized as pre-collapse, whereas stages III and IV indicate collapse and joint degeneration.
  • Stage I (pre-radiographic stage): The knee is symptomatic, but plain radiographs are normal; MRI or other advanced imaging is required to see the bone infarct.
  • Stage II (early osteonecrosis): Radiographs begin to show abnormalities such as subchondral cysts or sclerosis, but there is no subchondral fracture or articular surface collapse yet.
  • Stage III (collapse stage): A subchondral fracture is present, seen as the crescent sign on x-ray, and the articular surface is starting to collapse or flatten. No significant joint space narrowing exists, but the structural integrity is compromised.
  • Stage IV (arthritic stage): There is flattening of the condyle and secondary osteoarthritis changes including joint space narrowing, marginal osteophytes, subchondral sclerosis, and cysts.

Lesion size and location

In addition to these classification systems, clinicians also consider the size of the necrotic lesion and the extent to which the weight-bearing portion of the condyle is involved. As with osteonecrosis of the hip, larger lesions have a worse prognosis. For example, studies of SONK have shown that lesions occupying more than 40% to 50% of the femoral condyle surface are significantly more likely to progress to collapse and require surgery. A small lesion (<3.5 cm² or <20% of condyle width) might be managed nonoperatively with a chance of healing, whereas a large lesion (>5 cm² or >50% condyle involvement) has a high risk of collapse and often merits early surgical intervention. These considerations also apply to SON, although lesions in SON are often large or multifocal at presentation, reflecting the typically aggressive underlying etiologies.

Multifocal involvement

A unique aspect of SON is that patients may have multiple lesions in the same knee, such as both the femur and tibia condyles. Staging systems typically address the worst lesion. Multifocal osteonecrosis is characterized by involvement at 3 or more anatomical sites simultaneously; such extensive disease indicates a systemic process, such as high-dose steroids, and usually indicates a more challenging treatment course.

In summary, staging of SON is typically performed with the modified Ficat and Arlet classification in conjunction with an assessment of lesion size. Early-stage (I/II) disease is precollapse and potentially reversible or at least manageable with joint-sparing treatments. In contrast, late-stage (III/IV) disease involves bony collapse and often requires arthroplasty.

Prognosis

Prognosis and Complications

The prognosis for SON depends largely on the stage at diagnosis and the effectiveness of intervention.[20][32] Early-stage lesions have a better prognosis, whereas larger or later-stage lesions often progress to more severe degrees of joint destruction.[15]

• Early diagnosis improves outcomes: Stage I or II lesions managed with appropriate intervention may stabilize or resolve.
• Risk of progression: Roughly 80% of nonoperatively managed cases progress to advanced stages within a few years of diagnosis.
• Outcomes after arthroplasty: Total knee arthroplasty provides excellent pain relief and function in osteoarthritis (SON) cases, although younger patients face a higher likelihood of revision in the long term due to the prosthesis's limited lifespan.
• Multifocal disease prognosis: Patients with multifocal osteonecrosis often require multiple joint interventions, further compromising overall mobility.

Complications

Complications

• Disease-related: Subchondral collapse, secondary osteoarthritis, chronic pain, and progression to other joints.[2]
• Treatment-related: Joint-preserving surgeries can result in incomplete healing or progression of the lesion. TKA involves risks of infection, prosthetic loosening, and periprosthetic fractures, especially in immunosuppressed individuals.